Abstract

Obesity originates from an imbalance between caloric intake and energy expenditure that promotes adipose tissue expansion, which is necessary to buffer nutrient excess. Patients with higher visceral fat mass are at a higher risk of developing severe complications such as type 2 diabetes and cardiovascular and liver diseases. However, increased fat mass does not fully explain obesity’s propensity to promote metabolic diseases. With chronic obesity, adipose tissue undergoes major remodeling, which can ultimately result in unresolved chronic inflammation leading to fibrosis accumulation. These features drive local tissue damage and initiate and/or maintain multiorgan dysfunction. Here, we review the current understanding of adipose tissue remodeling with a focus on obesity-induced adipose tissue fibrosis and its relevance to clinical manifestations.

Figure 1

Adipose tissue progenitors (or precursors), often located in the vicinity of the vascular network, constitute a heterogeneous population. They can be discriminated through their capacity to differentiate into mature adipocytes and also by their level of commitment into the adipocyte differentiation program. The application of flow cytometry using various markers as well as single-cell RNA sequencing has enabled the identification of multiple cell populations. The CD9hi progenitors exhibited very limited adipogenic capacity with a high propensity for the production of extracellular matrix components. CD9hi progenitors include mesothelial cells, whose contribution in adipose tissue remodeling is currently unresolved. Further investigations are still needed to establish the relationship between these various populations of progenitors. In addition, a better understanding of the critical functional determinants and whether acquired phenotypes are reversible is needed.